Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss
With the advent of recent genetic technologies for mice, it is now feasible to investigate the circuit mechanisms of brain functions in an unprecedented manner. Although transgenic mice are commonly used on C57BL/6J (C57) background, hearing research has typically relied on different genetic backgro...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2019-02-01
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| Series: | Frontiers in Aging Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/article/10.3389/fnagi.2019.00029/full |
| _version_ | 1819083608063737856 |
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| author | Daniel Lyngholm Shuzo Sakata |
| author_facet | Daniel Lyngholm Shuzo Sakata |
| author_sort | Daniel Lyngholm |
| collection | DOAJ |
| description | With the advent of recent genetic technologies for mice, it is now feasible to investigate the circuit mechanisms of brain functions in an unprecedented manner. Although transgenic mice are commonly used on C57BL/6J (C57) background, hearing research has typically relied on different genetic backgrounds, such as CBA/Ca or CBA due to the genetic defect of C57 mice for early age-related hearing loss. This limits the utilization of available genetic resources for hearing research. Here we report congenic (>F10) Cre-dependent channelrhodopsin2 (ChR2) mice on CBA/Ca background. By crossing this line with Cre-driver mice on C57 background, F1 hybrids restored the hearing deficit of C57 mice. We also found a linear relationship between aging and hearing loss, with progression rates varied depending on genetic backgrounds (3.39 dB/month for C57; 0.82 dB/month for F1 hybrid). We further demonstrate that this approach allows to express ChR2 in a specific type of inhibitory neurons in the auditory cortex and that they can be identified within a simultaneously recorded population of neurons in awake mice. Thus, our Cre-dependent optogenetic transgenic mice on CBA/Ca background are a valuable tool to investigate the circuit mechanisms of hearing across lifespan. |
| first_indexed | 2024-12-21T20:35:16Z |
| format | Article |
| id | doaj.art-ba246c5213034f60a1db1a9e54bfc02a |
| institution | Directory Open Access Journal |
| issn | 1663-4365 |
| language | English |
| last_indexed | 2024-12-21T20:35:16Z |
| publishDate | 2019-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Aging Neuroscience |
| spelling | doaj.art-ba246c5213034f60a1db1a9e54bfc02a2022-12-21T18:51:08ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652019-02-011110.3389/fnagi.2019.00029424647Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing LossDaniel LyngholmShuzo SakataWith the advent of recent genetic technologies for mice, it is now feasible to investigate the circuit mechanisms of brain functions in an unprecedented manner. Although transgenic mice are commonly used on C57BL/6J (C57) background, hearing research has typically relied on different genetic backgrounds, such as CBA/Ca or CBA due to the genetic defect of C57 mice for early age-related hearing loss. This limits the utilization of available genetic resources for hearing research. Here we report congenic (>F10) Cre-dependent channelrhodopsin2 (ChR2) mice on CBA/Ca background. By crossing this line with Cre-driver mice on C57 background, F1 hybrids restored the hearing deficit of C57 mice. We also found a linear relationship between aging and hearing loss, with progression rates varied depending on genetic backgrounds (3.39 dB/month for C57; 0.82 dB/month for F1 hybrid). We further demonstrate that this approach allows to express ChR2 in a specific type of inhibitory neurons in the auditory cortex and that they can be identified within a simultaneously recorded population of neurons in awake mice. Thus, our Cre-dependent optogenetic transgenic mice on CBA/Ca background are a valuable tool to investigate the circuit mechanisms of hearing across lifespan.https://www.frontiersin.org/article/10.3389/fnagi.2019.00029/fulloptogeneticsneural circuitaginghearingauditory cortex |
| spellingShingle | Daniel Lyngholm Shuzo Sakata Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss Frontiers in Aging Neuroscience optogenetics neural circuit aging hearing auditory cortex |
| title | Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss |
| title_full | Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss |
| title_fullStr | Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss |
| title_full_unstemmed | Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss |
| title_short | Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss |
| title_sort | cre dependent optogenetic transgenic mice without early age related hearing loss |
| topic | optogenetics neural circuit aging hearing auditory cortex |
| url | https://www.frontiersin.org/article/10.3389/fnagi.2019.00029/full |
| work_keys_str_mv | AT daniellyngholm credependentoptogenetictransgenicmicewithoutearlyagerelatedhearingloss AT shuzosakata credependentoptogenetictransgenicmicewithoutearlyagerelatedhearingloss |